pubmed-article:10696997 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0389003 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C1565860 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C1705323 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0016884 | lld:lifeskim |
pubmed-article:10696997 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
pubmed-article:10696997 | pubmed:issue | 9204 | lld:pubmed |
pubmed-article:10696997 | pubmed:dateCreated | 2000-3-22 | lld:pubmed |
pubmed-article:10696997 | pubmed:abstractText | A new generation of non-steroidal anti-inflammatory drugs has been described that selectively targets the inducible isoform of cyclo-oxygenase, cyclo-oxygenase 2 (COX-2). This isoform is expressed at sites of inflammation, which has led to the speculation that its inhibition could provide all the benefits of current nonsteroidal anti-inflammatory drugs, but without their major side-effects on the gastrointestinal system (which are due to inhibition of COX-1). We have shown that COX-2 (identified by use of specific antibodies) is induced during the resolution of an inflammatory response, inhibition of COX-2 resulting in persistence of the inflammation due to the prevention of the synthesis of a range of anti-inflammatory prostanoids. We propose that there is a third isoform of this enzyme family, COX-3, a proposal that will have implication for the prescription of both existing and new generation anti-inflammatory drugs, and might represent a new therapeutic target. | lld:pubmed |
pubmed-article:10696997 | pubmed:language | eng | lld:pubmed |
pubmed-article:10696997 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10696997 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:10696997 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10696997 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10696997 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10696997 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10696997 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10696997 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10696997 | pubmed:month | Feb | lld:pubmed |
pubmed-article:10696997 | pubmed:issn | 0140-6736 | lld:pubmed |
pubmed-article:10696997 | pubmed:author | pubmed-author:WilloughbyD... | lld:pubmed |
pubmed-article:10696997 | pubmed:author | pubmed-author:MooreA RAR | lld:pubmed |
pubmed-article:10696997 | pubmed:author | pubmed-author:Colville-Nash... | lld:pubmed |
pubmed-article:10696997 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10696997 | pubmed:day | 19 | lld:pubmed |
pubmed-article:10696997 | pubmed:volume | 355 | lld:pubmed |
pubmed-article:10696997 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10696997 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10696997 | pubmed:pagination | 646-8 | lld:pubmed |
pubmed-article:10696997 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:10696997 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10696997 | pubmed:articleTitle | COX-1, COX-2, and COX-3 and the future treatment of chronic inflammatory disease. | lld:pubmed |
pubmed-article:10696997 | pubmed:affiliation | Department of Experimental Pathology, William Harvey Research Institute, St Bartholomew's and Royal London Hospital Schools of Medicine & Dentistry, UK. d.a.willoughby@mds.qmw.ac.uk | lld:pubmed |
pubmed-article:10696997 | pubmed:publicationType | Journal Article | lld:pubmed |
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